Papers associated with thyroid primordium (and slc26a4.3)

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	Hypo-functional SLC26A4 variants associated with nonsyndromic hearing loss and enlargement of the vestibular aqueduct: genotype-phenotype correlation or coincidental polymorphisms?, Choi BY., Hum Mutat. April 1, 2009; 30 (4): 599-608.
	[Evidence of a novel gene for the LAV-syndrome]., Birkenhäger R., Laryngorhinootologie. February 1, 2007; 86 (2): 102-6.
	[Identification of two heterozygous mutations in the SLC26A4/PDS gene in a family with Pendred-syndrome]., Birkenhäger R., Laryngorhinootologie. December 1, 2004; 83 (12): 831-5.
	Functional characterization of pendrin in a polarized cell system. Evidence for pendrin-mediated apical iodide efflux., Gillam MP., J Biol Chem. March 26, 2004; 279 (13): 13004-10.
	Pendrin is an iodide-specific apical porter responsible for iodide efflux from thyroid cells., Yoshida A., J Clin Endocrinol Metab. July 1, 2002; 87 (7): 3356-61.
	Functional differences of the PDS gene product are associated with phenotypic variation in patients with Pendred syndrome and non-syndromic hearing loss (DFNB4)., Scott DA., Hum Mol Genet. July 1, 2000; 9 (11): 1709-15.
	Human pendrin expressed in Xenopus laevis oocytes mediates chloride/formate exchange., Scott DA., Am J Physiol Cell Physiol. January 1, 2000; 278 (1): C207-11.
	The Pendred syndrome gene encodes a chloride-iodide transport protein., Scott DA., Nat Genet. April 1, 1999; 21 (4): 440-3.

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